Antifungal activity and mechanism of chitosan against Fusarium solani caused ginger soft rot during postharvest storage

Postharvest rot caused by Fusarium solani (F. solani) results in enormous economic loss to the global vegetables industry. Chitosan has been shown to be effective in control postharvest diseases of vegetables, but the specific mechanism of chitosan on F. solani has not been studied. In this study, we evaluated antifungal activity of chitosan against F. solani caused soft rot in vitro and in vivo. Antifungal assay results showed that chitosan significantly inhibited the mycelial growth and spore germination of F. solani. Simultaneously, chitosan showed disruptive activity on the mycelial morphology and cell membrane, which were achieved by decreasing intracellular sugars, proteins and lipids content. Furthermore, chitosan treatment significantly decreased tricarboxylic acid (TCA)-related enzymes activity, reducing the number of metabolites in the TCA cycle. UPLC-Triple-TOF/MS-based metabolomics analysis showed that chitosan interferes with fungal metabolic pathways, mainly related to energy metabolism, lipid metabolism and sugar metabolism. Exogenous α-D-glucose and linoleic acid treatment promoted mycelia growth, verifying the sugar catabolism and TCA cycle was involved in the inhibition of chitosan against F. solani. The in vivo study showed that chitosan treatment effectively reduced disease rate and severity of postharvest soft rot through activating the biochemical defense response and modulating the expression of phytopathogenic responses LysM genes. These results contribute to explore the underlying mechanisms of chitosan against F. solani.